ライフサイエンスコーパス: beta-COP

1 beta-COP and several Galpha subunits (Galpha(i1-3), Galp

2 se II, p58, trans-Golgi network (TGN)38, and beta-COP and is distinct from the endoplasmic reticulum

3 on of the RNA-binding proteins as alpha- and beta-COP.

4 of Cdc42Hs while, as is the case for ARF and beta-COP, expression of a GTPase-deficient form of ARF (

5 t proteins ADP-ribosylation factor (ARF) and beta-COP, the perinuclear clustering of Cdc42Hs is rapid

6 rms partially co-localized with calnexin and beta-COP, markers of the endoplasmic reticulum and the G

7 ts from both cerebellum and COS-7 cells, and beta-COP protein interacted directly with immobilized KA

8 fically interacts with at least zeta-COP and beta-COP of the COPI coatomer complex.

9 delta-COP at a site common to the gamma- and beta-COP subunits.

10 cPLA(2) results in dispersion of giantin and beta-COP from their normal, condensed Golgi localization

11 BIG2 were recovered in the same fraction as beta-COP, a marker for Golgi membranes.

12 verlaps with cellular Golgi proteins such as beta-COP and GS-28, G(C) expressed in the absence of G(N

13 se-dependent decrease in membrane-associated beta-COP when incubated with rapidly sedimenting membran

14 increase in the level of membrane-associated beta-COP.

15 otifs: an N-terminal dibasic site that binds beta-COP to hold channels in ER and a C-terminal "releas

16 ulture cells demonstrated directly that both beta-COP and delta-COP, but no other coatomer subunits,

17 bution of pre-Golgi intermediates containing beta-COP.

18 ia an intermediate compartment that contains beta-COP, which is best known as a component of the COPI

19 PI and CFTR in epithelial cells, we depleted beta-COP from the human colonic epithelial cell HT-29Cl.

20 The ability to enhance beta-COP membrane binding was not limited to the peptide

21 uds were observed and buds were labelled for beta-COP.

22 n addition, we demonstrate a requirement for beta-COP as a cellular cofactor for Nef that was necessa

23 esicles that contained Rab2, PKCiota/lambda, beta-COP, and p53/p58.

24 aptophysin colocalized with the Golgi marker beta COP in elongated cytoplasmic compartments that exte

25 hase, and caused dispersion of Golgi markers beta-COP and GM130, whereas ER structure appeared intact

26 e membranes contained a negligible amount of beta-COP that was reflected by the drastic reduction in

27 tif, and shows mutually exclusive binding of beta-COP and 14-3-3beta on adjacent N-terminal sites.

28 ssay was used to measure membrane binding of beta-COP when incubated with the mutant.

29 functional consequence as cells depleted of beta-COP showed decreased cAMP-activated chloride curren

30 by altered immunofluorescent distribution of beta-COP and reduced efflux of BODIPY C5-ceramide, a pho

31 rmation of Golgi stacks, the distribution of beta-COP, or the transport and surface display of E-cadh

32 The observed pI of beta-COP was sensitive to alkaline phosphatase digestion

33 membranes were evaluated for the presence of beta-COP.

34 necessary for the downstream recruitment of beta-COP and release of Rab2-mediated retrograde-directe

35 assay was employed to measure recruitment of beta-COP to membrane when incubated with the Rab2 (13-me

36 I is compromised, as shown by the release of beta-COP into the cytosol.

37 defects in ldlF cells, and the stability of beta-COP is not linked directly to that of epsilon-COP.

38 ing antibodies against myocilin, tubulin, or beta-COP (a specific golgi protein) or vital stains for

39 nectin with the Golgi membrane markers p115, beta-COP, and the trans-Golgi network marker, syntaxin 6

40 combinant Rab2 protein to the assay promoted beta-COP membrane association.

41 egulator, ArfGAP2/3, and the adaptor protein beta-COP-enable GIV to coordinately regulate Arf1 signal

42 de isomerase (PDI) and the COPI coat protein beta-COP.

43 downstream recruitment of beta-coat protein (beta-COP) to VTCs, the Rab2-PP2-treated membranes were e

44 K-ATPase alpha-subunit and the coat protein, beta-COP, a component of the COP-I complex.

45 Because Rab2, beta-COP, and p53/p58 are marker proteins for pre-Golgi

46 These vesicles contained Rab2, beta-COP, p53/gp58, and protein kinase Ciota/lambda but

47 slowly sedimenting vesicles containing Rab2, beta-COP, and p53/gp58 but lacking anterograde grade-dir

48 Based on numerous observations that show (beta-COP) GAPDH associates with cytoskeletal elements, w

49 Moreover, some beta-COP colocalizes with intracellular caveolin-1, whic

50 refeldin A, except that the coatomer subunit beta-COP remained on Golgi-derived membrane tubules.

51 s in ldlF cells of another coatomer subunit, beta-COP, and the peripheral Golgi protein ldlCp were no

52 s well as that of a second coatomer subunit, beta-COP.

53 hosphorylation-dependent fashion to suppress beta-COP binding and allow forward transport.

54 rogeneity was observed, particularly for the beta-COP and delta-COP subunits.

55 the Rab2 peptide on the distribution of the beta-COP subunit of coatomer because COPI partially loca

56 late with increased intracellular binding to beta COP proteins.

57 Depletion of S-100 with the antibody to beta-COP confirmed that the coatomer was the sole protei

58 ly synthesized alpha-subunit associates with beta-COP immediately after its synthesis but that this i

59 PI vesicles was based on colocalization with beta-COP, a marker for these vesicles.

60 and (d) showed extensive colocalization with beta-COP.

61 unoelectron microscopy, GIV colocalizes with beta-COP and Galpha(i3) on vesicles found in close proxi

62 it, the alpha-subunit does not interact with beta-COP and traffics to the plasma membrane.

63 The interaction with beta-COP was reduced by mutating a dibasic motif at Lys(

64 the Na,K-ATPase alpha-subunit interacts with beta-COP, is retained in the endoplasmic reticulum, and

65 The mutant protein does not interfere with beta-COP binding but stimulates the release of slowly se